Psychosomatic Medicine
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ladwig, K.-H.
Right arrow Articles by Schmitt, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ladwig, K.-H.
Right arrow Articles by Schmitt, C.
Related Collections
Right arrow Stress and Coping
Right arrow Other Cardiovascular Medicine
Psychosomatic Medicine 65:222-228 (2003)
© 2003 American Psychosomatic Society

ORIGINAL ARTICLES

Exaggerated Electrodermal Startle Responses After Intracardiac Shock Discharges in Patients With Implanted Cardioverter Defibrillators

Karl-Heinz Ladwig, PhD, MD, Birgitt Marten-Mittag, Dipl Soc, Isabel Deisenhofer, MD, Birgit Hofmann, Johannes Schapperer, Sonja Weyerbrock, MD and Claus Schmitt, MD

From the Institut und Poliklinik für Psychosomatische Medizin (K.H.L., B.M-M., B.H., J.S.), Med. Psychologie und Psychotherapie des Klinikums Rechts der Isar der Technischen Universität München; National Research Centre for Environment and Health (GSF), GSF-Institute of Epidemiology (K.H.L.); and Deutsches Herzzentrum München (I.D., S.W., C.S.), Klinik an der Technischen Universität München, München, Germany.

Address reprint requests to: K. H. Ladwig, PhD, MD habil., Institut u. Poliklinik für Psychosomatische, Medizin, Psychotherapie u. Med. Psychologie, Universitätsklinikum rechts der Isar der TUM, Langerstraße 3, 81675 München, Germany. Email: kh.ladwig{at}lrz.tu-muenchen.de


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
OBJECTIVE: We studied whether repetitive intracardiac shock discharges of implantable cardioverter defibrillators (ICDs) provoke an enduring enhancement of startle responses.

METHODS: The study population comprised 134 patients with an ICD. Among those, 67 patients had experienced shock delivery. Thirty-five patients had received five or more shocks. We used the startle reflex paradigm, which consisted of 15 acoustic stimuli (95 dB, 1000 Hz, 500 ms duration). Skin conductance response was measured using a constant 0.5 V through 8-mm electrodes placed on each subject’s nondominant palm. Response magnitude was calculated by subtracting the baseline response level of the 2 seconds immediately preceding tone onset from the maximum response level within 1 to 4 seconds after tone onset. The left orbicularis oculi electromyogram (EMG) response was calculated by subtracting the mean EMG level during the 2 seconds immediately preceding tone onset from the highest EMG level measured within 40 to 200 ms after tone onset. Habituation was defined by the response slope of the regression equation and by the number of trials required to reach the nonresponse criterion.

RESULTS: Although EMG response measures of magnitude and habituation failed to yield differences between study groups, patients who had experienced five or more ICD shocks exhibited a significantly larger skin conductance response magnitude in comparison to the patients who had experienced fewer than five shocks (median, interquartile range: 0.364, 0.209–0.618 vs. 0.512, 0.375–0.791; Mann-Whitney U test, p = .007). Poorer habituation in the group with five or more shocks in comparison with the low shock group was confirmed both by the number of trials needed to reach the nonresponse criterion (median, interquartile range: 10, 5–14 vs. 5, 2–13; p = .003) and by the response slope (median, interquartile range: 0.209, 0.116–0.274 vs. 0.262, 0.181–0.332; p = .008). After controlling for potential confounding factors (age, anxiety, aversiveness of stimuli, time since last shock experience, and use of ß-adrenoceptor antagonists), intracardiac shock discharges had the strongest impact on augmented skin conductance response magnitude (adjusted odds ratio = 3.0, 95% confidence interval = 1.3–7.2, p = .01) and impaired habituation (adjusted odds ratio = 2.8, 95% confidence interval = 1.2–6.3; p = .015).

CONCLUSIONS: Intracardiac shock discharges are associated with augmented skin conductance responses and slower habituation, indicating sustained sympathetic arousability, which is presumably centrally mediated.

Key Words: implantable cardioverter defibrillator, • startle reflex, • shock sensitization, • skin conductance response, • electromyogram response.

Abbreviations: ASR = acoustic startle reflex;; EDA = electrodermal activity;; EMG = electromyogram;; EMR = electromyographic response;; HADS = Hospital Anxiety and Depression Scale;; ICD = implanted cardioverter defibrillator;; IQR = interquartile range;; PTSD = posttraumatic stress disorder;; SC = skin conductance;; SCR = skin conductance response.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
A significant proportion of patients at risk for sudden cardiac death fail to respond to pharmacological therapy. In these patients, treatment with implanted cardioverter defibrillators (ICDs) has become an effective strategy for managing life-threatening ventricular arrhythmias (1).

The introduction of the device has been accompanied by research on psychological adjustment and quality of life of ICD patients (2–14) . The overall results of these investigations reveal a positive acceptance of ICD technology. Despite their serious disease condition, ICD patients have also achieved sufficient quality-of-life levels with the help of the device (2–6, 14) . Mean anxiety scores of ICD patients have often been found to be lower than those of cardiac patients without ICDs (2, 4–6, 14) , which may reflect the feeling of security conferred by the device. ICD patients apparently appreciate the effective protection against malignant arrhythmias.

In clinical observations and single case studies, a minority of ICD patients exhibited a pronounced and clinically relevant maladaptation (7–15) . Kowey (7), for example, described fear, loss of hope, and a wish to die in ICD patients. Maladaptation is often caused by factors intrinsic to the individual. However, shock delivery itself may contribute to the suffering of these patients (10–13, 15) . These studies also showed that accumulating shock delivery is associated with a dramatic increase in the frequency of preoccupation with anticipatory anxiety. According to these data, increasing numbers of ICD shocks are associated with a dramatic increase in the number of patients preoccupied by anticipatory anxiety. The repetitive perception of five or more shocks has been considered as a critical borderline for emotional distress (10, 11, 13) .

To date it has not been proven whether repetitive shock discharges in patients give rise to sustained sympathetic arousability, a distress condition that may further enhance susceptibility to ventricular tachycardia through persistent exaggerated autonomic arousal (16, 17) . To address this question, we used the acoustic startle reflex (ASR) paradigm. The ASR is a ubiquitous, cross-species reaction to an abrupt and intense but otherwise neutral stimulus, characterized by a sequence of flexor motor movements and autonomic nervous system changes. ASR is processed with short latency by a simple polysynaptic brainstem mechanism (18) with further cortically mediated modulations distant from the primary startle pathway itself (19–21) . Thus, the ASR is appealing for noninvasive assessment of neural reactivity in response to severe stress.

There is ample evidence to confirm that ASR is markedly increased in the presence of cues that have been previously paired with shock (22), as well as in aversive environments that are likely to provoke anticipatory anxiety (23), in subjects with high and low levels of fearfulness (24) and in patients with anxiety disorders (25). Exaggerated startle responses have been demonstrated as a criterion symptom for the persistent presence of increased arousal in subjects in the aftermath of traumatic events (26).

The startle reflex is not only increased by aversive learning. Repetitive delivery of shocks itself enhances the amplitude of the startle responses in nonhuman (27, 28) and human subjects (29) and may lead to sensitization. Basically, shock sensitization refers to the potentiation of a startle response in subjects given a series of shocks compared with subjects not given the shock. Thus, shock sensitization might be the precondition of aversive learning (29).

The repetitive delivery of intracardiac shocks may put patients under conditions that resemble a state of shock sensitization. We therefore expected both larger magnitude responses and slower habituation, as measured by startle-evoked electrodermal responses and electromyographic responses (EMRs), in patients who had received more than five ICD shocks.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Participants
We recruited 149 consecutive ICD patients who attended the cardiology outpatient clinic of the Deutsches Herz Zentrum München for routine ICD checkups. Patients were not included if the first ICD implantation had occurred less than 3 months earlier. Patients who suffered from severe cognitive impairment (two cases) or had a defined hearing loss (>40 dB in five distinct frequency bands; six cases) were excluded from the analysis. In seven cases, physiological data were incomplete. Thus, the study population comprised 134 patients. Written informed consent was obtained from all patients. The study was approved by the ethics committee of the medical faculty of the Technische University of Munich.

The clinical characteristics of the patients are given in Table 1. The study group comprised 67 patients without any device discharge and 67 patients who had experienced a shock discharge. Among shock recipients, 35 patients had received five or more shocks.


View this table:
[in this window]
[in a new window]
  		TABLE 1. Description of the Study Population (N = 134), Stratified for Three Shock Groups
 
Psychophysiological Procedure
The room temperature was held constant at 22°C, and humidity was kept at 55%. Patient investigations were carried out between 9:00 AM and 1:00 PM. Subjects underwent a hearing test and received standard instructions while the electrodes were attached in accordance with published recommendations (30, 31) .

We applied the ASR paradigm proposed by Shalev et al (26). It comprised 15 loud tones as independent variables (trials). The acoustic startle stimulus was a 500-ms burst of 1000 Hz with a nearly instantaneous rise time presented binaurally through headphones (Panasonic). The intensity of the acoustic stimulus was 95 dB. Intertrial intervals were randomly selected and ranged from 17 to 32 seconds.

Dependent variables of the ASR paradigm were the EMR (to assess sensorimotor responses) and the skin conductance response (SCR). Heart rate was measured, and average responses were analyzed; heart rate variability was not assessed. Initial analyses of heart rate showed a complex response pattern requiring further evaluation. Given this, we chose to present only skin conductance (SC) and electromyographic (EMG) indices of startle in this report. Signals were amplified and filtered by a bioamplifier (B-scope, Regensburg, Germany).

SC was measured directly by a coupler using a constant 0.5 V through 8-mm (sensor diameter) electrodes (Beckman-type Ag/AgCl) placed on the subject’s nondominant palm. SC was analyzed in a spectrum from 15.9 mHz to 10 Hz and digitalized at 50 Hz. Response magnitude of the startle stimulus for each trial was defined by subtracting the average SC for the 2 seconds immediately preceding tone onset from the maximum level within 1 to 4 seconds after tone onset. SC was measured in microsiemens (µsiemens). SCR scores were square root transformed before analysis to reduce the variance associated with unusually large responses. As a global measure of SCR, the average SCR across all 15 trials (SCR1–15) was used.

The left orbicularis oculi EMG signal was recorded through 4-mm (sensor diameter) surface electrodes (Beckman-type Ag/AgCl) and filtered to retain a 90- to 500-Hz frequency range. Sampling frequency was 1000 Hz. EMG1–15 data were measured in microvolts (µV) and ranged from 0.991 to 16.871 (square root transformed). Response magnitude of the startle stimulus was defined by subtracting the mean EMG level during the 2 seconds immediately preceding tone onset from the highest EMG level measured within 40 to 200 ms after tone onset.

Habituation was defined in two ways: 1) By the response slope of the regression equation Y = bX + a for trials 2 through 15, where Y is the magnitude of the response and X is the log trial number. To control for the individual level of response, the absolute value of the slope, b, was divided by the intercept, a, of the regression line. 2) By trials to nonresponse: an SCR <= 0.15 µsiemens (nontransformed) and an EMG level of 18 µV (nontransformed) were considered to constitute a nonresponse. A patient was considered to be nonresponsive (habituated) when the SCR/EMG nonresponse criteria were met in two consecutive trials.

Anxiety and depression were evaluated using the 14-item Hospital Anxiety and Depression Scale (HAD) (32) with published norms obtained from a standard German population with coronary artery disease (33). The HADS has four options for each item with a scoring range of 0 to 3; seven items cover anxiety, and seven items cover depressive symptoms. The responses were scored on a Likert scale. Scores ranged from 0 to 21 for each subscale; a score >8 indicated heightened distress. Aversiveness of auditory stimuli was rated on a one-item scale with three options (low, medium, and high).

Statistics
We used nonparametric statistical tests to test for group differences because the SCR measures were not normally distributed (one-sample Kolmogorov-Smirnov test, p <= .05). We defined a subgroup of patients who experienced five or more shocks and compared this index group with patients experiencing zero to four shocks because we expected five or more shocks to be the borderline for maladaptation. We also analyzed patients with zero shocks, one to four shocks, and five or more shocks to assess a possible dose-effect relation. To this end, the Jonckheere-Terpstra test was used to calculate the dose-effect relation of SCR1–15 with multiple shock experience and with age groups.

We used logistic regression models to study the independent influence on SCR magnitude and habituation (both "split-half" dichotomized), incorporating the following predictors: 1) less than five shocks vs. five or more shocks, 2) age (continuous), 3) anxiety level (dichotomized), 4) use of ß-adrenoceptor antagonists, 5) rating of aversiveness of auditory stimuli (dichotomized), and 6) time since last shock experience. Backward stepwise selection and likelihood ratio statistics were used to select variables for removal. All analyses were performed using SPSS for Windows (version 10.0).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Analysis of SCR Magnitude
The analysis of SCR magnitude over all 15 trials (SCR1–15; range = 0.015–1.580 µsiemens, square root transformed) confirmed the hypothesis that patients who had received five or more shocks (N = 35) by the ICD device showed larger SCR magnitude than patients who had received fewer than five shocks (N = 99): the median SCR1–15 (and IQR) was 0.512 (0.375–0.791) in the high shock group and 0.364 (0.209–0.618) in the low shock group (Mann-Whitney U test, p = .007). Figure 1 displays mean differences in both groups for each trial and demonstrates significant differences for all but the first two trials.



View larger version (19K):
[in this window]
[in a new window]
  		Fig 1. Median SCRs for each of the 15 tone trials, stratified for the low shock group (<5 shocks, N = 99 patients) and the high shock group (>=5 shocks, N = 35 patients). The graph demonstrates significantly heightened median values for all but the first two trials. Error bars represent the 25th percentile in the low shock group and the 75th percentile in the high shock group (Mann-Whitney U test: *p < .10; **p < .05; ***p < .01).

 
Stratification of patients into three shock groups (no shocks, one to four shocks, five or more shocks) disclosed a dose-effect relationship of shock experience on SCR1–15 magnitude (Jonckheere-Terpstra test, p = .017).

Table 2 shows that other factors influenced SCR magnitude as well: SCR1–15 magnitude was augmented in patients with heightened anxiety but, against our expectations, did not reach significance. Tone aversiveness was significantly associated with higher SCR1–15 magnitude, indicating greater involvement or hypervigilance. As expected, ß-adrenoceptor antagonists had no influence on SCR magnitude.


View this table:
[in this window]
[in a new window]
  		TABLE 2. Group Differences of SCR Magnitude and Habituation in the ICD Study Group (N = 134)a
 
Shock sensitization to startle in the animal model tends to normalize with the passage of time. We therefore evaluated whether SCR1–15 was influenced by the time since the last shock experience. In 55 (of 67) patients with shock experience, valid information was available: the median time was 369 days (range, 6–1750 days). We separated patients into groups of <=369 days and >369 days and found no differences in SCR1–15. This finding indicates that shock sensitization in ICD patients remains stable over time (see Table 2).

SCR1–15 values were significantly less pronounced in older age groups (Jonckheere-Terpstra test, p = .002), whereas the occurrence of shocks was uninfluenced by age. The relationship between SCR1–15 and the three shock groups (no shocks, one to four shocks, five or more shocks) remained relatively constant over the four different age groups, although the age groups had different mean magnitude levels.

In the logistic regression model using split-half dichotomized SCR1–15 as the outcome (incorporating shock groups, age, anxiety, tone aversiveness, time since last shock, and use of ß-adrenoceptor antagonists), patients who had experienced five or more shocks had a three-fold higher risk for high startle responses: adjusted odds ratio = 3.0 (95% CI: 1.3–7.2, p = .01). Patients who exhibited anxiety had a 2.4-fold higher risk: adjusted odds ratio = 2.4 (95% CI: 1.0–5.5, p = .04). None of the other factors reached significance.

Analysis of SCR Habituation
The repeated presentation of acoustic stimuli generally results in a continuous decrease in SCR in a negatively accelerated manner. We analyzed whether the ability to cease responding to repetitive stimuli was impaired in patients who had experienced intracardiac shock delivery. The number of trials to reach the nonresponse criteria confirmed poorer habituation in the high shock group in comparison with the low shock group (p = .003). Table 2 shows that the modified slope of the habituation line for trials 2 through 15 also yielded a significant mean difference in habituation (low values indicate impaired habituation) between the low shock group in comparison with the high shock group (p = .008).

In the logistic regression model (split-half dichotomized modified habituation slope), only the experience of five or more shocks remained as a significant covariate (p = .015) with an adjusted odds ratio of 2.8 (95% CI: 1.2–6.3).

Analysis of EMR Magnitude and Habituation
The analysis of the mean orbicularis oculi EMG measures (EMR1–15) failed to yield differences between patients in whom the ICD device had delivered five or more shocks (N = 35) and patients who had experienced fewer than five shocks: the median EMR1–15 (IQR) was 4.70 (3.20–7.01) in the high shock group and 4.40 (3.50–6.93) in the low shock group (N = 99) (Mann-Whitney U test, p = .950). The number of trials to reach the nonresponse criteria for EMR in the high shock group in comparison with the low-shock group (median (IQR): 6 (3–14) vs. 4 (2–14); Mann-Whitney U test, p = .491) revealed no group differences, nor did the modified slope of the habituation line for trials 2 through 15 (Mann-Whitney U test, p = .629).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
ACKNOWLEDGMENTS
 REFERENCES
 
The major finding of the present study was a significant and independent influence of intracardiac shock discharges on exaggerated SC startle response magnitude and of impaired SCR habituation after repeated presentation of the startling stimulus. Patients who had experienced more than five ICD firings had larger SCRs to startle stimuli. It is unlikely that a shock can generate a state of arousal that persists for a long time. However, SCR magnitudes were elevated no matter how long it had been since the last shock. These results point to a sustained increased sympathetic arousability acquired through shock delivery and mediated by central nervous influences (18–20) . According to these findings, ICD shock delivery can increase arousability to intense punctate stimuli, with more shocks leading to a greater increase in reactivity without a significant increase in background arousal.

We consider the SCR data to reflect the sympathetic component of the autonomic startle reaction pattern since neural control of SCR is exerted exclusively through the sympathetic branch of the autonomic nervous system (34). ß-Adrenergic influences are still not likely because sympathetic effects of the sweat glands involve cholinergic (not adrenergic) neurotransmission (34).

Neurophysiologically, these patients enter a persistent steady state of increased preparation for responding and are less able to ignore stimuli that have lost their novelty. The sympathetic arousability may mirror psychopathological states like anxiety, depression, and profound helplessness, which have recently been linked to shock delivery (10–13) . Nevertheless, the results do not simply reflect the neurophysiological component of augmented anxiety states in ICD patients, because the effect size of anxiety in the multivariate model was considerably lower in comparison with the influence of intracardiac shock discharges. Randomly delivered ICD shocks apparently promote a state of enduring anticipation of experiencing uncontrollable, painful interoceptive stimuli, which has been shown experimentally to be a strong promoter of exaggerated startle (6–9) . However, the sustained elevated readiness of sympathetic arousal acts neurophysiologically beyond an overt aversive affective state. Thus, the exaggerated electrodermal activity (EDA) response pattern might be the "precondition of aversive learning" (29) and might reflect the psychobiological component of individual vulnerability (15), which determines the amount of stress needed for affective maladaptation.

Evidence in the literature indicates that the experience of five or more repetitive shocks is the "cutoff" for subsequent affective maladaptation: Lüderitz et al. (10) showed that patients receiving more than five shocks had a significant increase in anxiety during the 12-month-follow-up period after ICD implantation. Herrmann et al. (11) revealed a clear association between the number of ICD shocks and the frequency of patients suffering from anxiety and depression, comparing patients who had received 0 to 4 shocks, 5 to 9 shocks, and >=10 shocks. Heller et al. (13) found that the experience of five or more ICD shocks was strongly associated with increased health concern, sadness, fatigue, and nervousness. Interestingly, the present data yielded a dose-effect relation and confirmed five shocks to be the borderline for impaired sympathetic adaptation.

Augmented sympathetic activity has been repeatedly demonstrated to enhance susceptibility to ventricular tachycardia (16, 17) by acting on the electrophysiological properties and contractile functions of the heart (35).Thus, the initially life-saving shock discharges of the ICD may provoke a fatal circulus vitiosus by lowering the threshold for the release of ventricular tachycardia/ventricular fibrillation in these patients.

Eye-blink startle magnitude is by far the most common measure of startle in humans (36). Nevertheless, the present study revealed no group effects of the orbicularis EMG measures, most likely because of the absence of state fear/anxiety-inducing stimuli. Hamm et al. (25) studied blink modulation and autonomic response patterns in animal and mutilation fearful subjects. They applied an acoustic startle that produced stimuli of 105 dB of white noise in fear-relevant neutral and pleasant scenes. Blink magnitude did not differ between in high animal-fearful patients and control subjects when watching neutral slides. The EMR enhancement was specific to fear-relevant content.

In a preliminary clinical study of patients with posttraumatic stress disorder on the eye-blink component of the startle reflex to repeated affectively neutral tactile and auditory stimuli, Ross et al. (37) found no group effect for EMR habituation. This finding was confirmed by Shalev et al. (26), who studied physiological responses to loud tones in patients with PTSD, patients with anxiety disorders, and mentally health subjects. They revealed a strong effect for EDA but not for EMG response measures in PTSD patients. Orr et al. (38) replicated these findings and also found significant EDA response patterns and insignificant EMG responses in the startle paradigm. They concluded that a possible explanation for the lack of significance for EMG responses may be the absence of an emotional state sufficient to modulate the startle response. The observation of an exaggerated muscular startle response may depend on the actual presence of a sufficiently strong negative emotional state such as (state) anxiety.

The present study has some limitations. Because of the cross-sectional design, we cannot completely rule out that the elevated physiological responses are constitutional and not acquired through shock discharges. However, this is not supported by the observed dose-effect relationship. This study did not include measurements of heart rate variability. Because measurements of heart rate variability could be useful for assessing the relative potential contribution of sympathetic and parasympathetic nerve activity, this approach should be used in further investigations of changes in autonomic activity after shock delivery in ICD populations.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
REFERENCES
 
This research project was supported in part by a research grant from the Medical Faculty of the Technische Universität München (KKF-H 18-97) and by a nonrestricted research grant from Guidant Medical Devices (both grants to Dr. Ladwig). We are indebted to Raymonde Busch, Dipl. Math., IMSE Epidemiology Department, Technische Universität München, and to Terry Blumenthal, PhD, Department of Psychology, Wake Forest University, for their valuable advice in the preparation of this manuscript.

Received for publication May 10, 2001.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. Zipes DP, Wyse DG, Friedman PL, Epstein AE, Halstrom AP, Greene HL, Schron EB, Domanski M. A comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med 1997; 337: 1576–83.[Abstract/Free Full Text]
  2. Vlay SC, Olson LC, Fricchione GL, Friedman R. Anxiety and anger in patients with ventricular tachyarrhythmias: responses after automatic internal cardioverter defibrillator implantation. PACE Pacing Clin Electrophysiol 1989; 12: 366–73.[CrossRef][Medline]
  3. Pycha C, Dalegulledge A, Hutzler J, Kadri N, Maloney J. Psychological responses to the implantable defibrillator: preliminary observations. Psychosomatics 1986; 27: 841–5.[Abstract/Free Full Text]
  4. Lüderitz B, Jung W, Deister A, Marneros A, Manz M. Patient acceptance of the implantable cardioverter defibrillator in ventricular tachyarrhythmias. PACE Pacing Clin Electrophysiol 1993; 16: 1815–21.[CrossRef][Medline]
  5. May CD, Smith PR, Murdock CJ, Davis MJE. The impact of the implantable cardioverter defibrillator on quality of life. PACE Pacing Clin Electrophysiol 1995; 18: 1411–8.[CrossRef][Medline]
  6. Chevalier P, Verrier P, Kirkorian G, Touboul P, Cottraux J. Improved appraisal of the quality of life in patients with automatic implantable cardioverter defibrillator: a psychometric study. Psychother Psychosom 1996; 65: 49–56.[CrossRef][Medline]
  7. Kowey PR. The calamity of cardioversion of conscious patients. Am J Cardiol 1988; 61: 1106–7.[CrossRef][Medline]
  8. Fricchione GL, Olson LC, Vlay SC. Psychiatric syndromes in patients with the automatic internal cardioverter defibrillator: anxiety, psychological dependence, abuse, and withdrawal. Am Heart J 1989; 117: 1411–4.[CrossRef][Medline]
  9. Sears SF, Conti JB, Curtis AB, Saia TL, Foote R, Wen F. Affective distress and implantable cardioverter defibrillators: cases for psychological and behavioral interventions. PACE Pacing Clin Electrophysiol 1999; 22: 1831–4.[CrossRef][Medline]
  10. Lüderitz B, Jung W, Deister A, Manz M. Patient acceptance of implantable cardioverter defibrillator devices: changing attitudes. Am Heart J 1994; 127: 1179–84.[CrossRef][Medline]
  11. Herrmann C, Mühen VF, Schaumann A, Buss U, Kemper S, Wantzen C, Gonska BD. Standardized assessment of psychological well-being and quality of life in patients with implanted defibrillators. PACE Pacing Clin Electrophysiol 1997; 20: 95–103.[CrossRef][Medline]
  12. Bourke JP, Turkington D, Thomas G, McComb JMM, Tynan M. Florid psychopathology in patients receiving shocks from implanted cardioverter-defibrillators. Heart 1997; 78: 581–3.[Abstract/Free Full Text]
  13. Heller SS, Ormont MA, Lidagoster L, Sciacca RR, Steinberg JS. Psychosocial outcome after ICD implantation. PACE Pacing Clin Electrophysiol 1998; 21: 1207–15.[CrossRef][Medline]
  14. Pauli P, Wiedemann G, Dengler W, Blaumann-Benninghoff G, Kühlkamp V. Anxiety in patients with an automatic implantable cardioverter defibrillator: what differentiates them from panic patients? Psychosom Med 1999; 61: 69–79.[Abstract/Free Full Text]
  15. Godemann F, Ahrens B, Behrens S, Bertold R, Gandor C, Lampe F, Linden M. Classic conditioning and dysfunctional cognitions in patients with panic disorder and agoraphobia treated with an implantable cardioverter/defibrillator. Psychosom Med 2001; 63: 231–8.[Abstract/Free Full Text]
  16. Lown B, DeSilva RA, Reich P, Murawski BJ. Psychophysiologic factors in sudden cardiac death. Am J Psychiatry 1980; 137: 1325–35.[Abstract/Free Full Text]
  17. Verrier RL, Lown B. Behavioural stress and cardiac arrhythmias. Annu Rev Physiol 1984; 46: 155–76.[CrossRef][Medline]
  18. Lee Y, Lopez DE, Meloni EG, Davis M. A primary acoustic startle pathway: obligatory role of cochlear root neurons and the nucleus reticularis pontis caudalis. J Neurosci 1996; 16: 3777–89.
  19. Rosen JB, Davis M. Enhancement of acoustic startle by electrical stimulation of the amygdala. Behav Neurosci 1988; 102: 195–202.[CrossRef][Medline]
  20. Hitchcock JM, Davis M. The efferent pathway of the amygdala involved in conditioned fear as measured with the fear potentiated startle paradigm. Behav Neurosci 1991; 105: 826–42.[CrossRef][Medline]
  21. Campeau S, Davis M. Involvement of the central nucleus and basolateral complex of the amygdala in fear conditioning measured with fear-potentiated startle in rats trained concurrently with auditory and visual conditioned stimuli. J Neurosci 1995; 15: 2301–11.[Abstract]
  22. Brown JS, Kalish HL, Farber IE. Conditional fear as revealed by magnitude of startle response to an auditory stimulus. J Exp Psychol 1951; 41: 317–28.[CrossRef][Medline]
  23. Grillon Ch, Ameli R, Woods SW, Merikangas K, Davis M. Fear-potentiated startle in humans: effects of anticipatory anxiety on the acoustic blink reflex. Psychophysiology 1991; 28: 588–95.[Medline]
  24. Cook EWIII, Davis TL, Hawk LW, Spence EL, Gautier CH. Fearfulness and startle potentiation during aversive visual stimuli. Psychophysiology 1992; 29: 633–45.[Medline]
  25. Hamm AO, Cuthbert BN, Globisch J, Vaitl D. Fear and the startle reflex: blink modulation and autonomic response patterns in animal and mutilation fearful subjects. Psychophysiology 1997; 34: 97–107.[Medline]
  26. Shalev AY, Scott PO, Peri T, Schreiber S, Pitman RK. Physiologic responses to loud tones in Israeli patients with posttraumatic stress disorder. Arch Gen Psychiatry 1992; 49: 870–5.[Abstract/Free Full Text]
  27. Boulis NM, Davis M. Footshock-induced sensitization of electrically elicited startle reflexes. Behav Neurosci 1989; 103: 504–8.[CrossRef][Medline]
  28. Davis M. Sensitization of the acoustic startle reflex by footshock. Behav Neurosci 1989; 103: 495–503.[CrossRef][Medline]
  29. Hamm AO, Stark R. Sensitization and aversive conditioning: effects on the startle reflex and electrodermal responding. Integr Phys Behav Sci 1993; 28: 171–6.[Medline]
  30. Fridlund AJ, Cacioppo JT. Guidelines for human electromyographic research. Psychophysiology 1986; 23: 567–89.[Medline]
  31. Fowles DC, Christie MJ, Edelberg R, Grings WW, Lykken DT, Venables PH, Publication recommendations for electrodermal measurements. Psychophysiology 1981; 18: 232–9.[Medline]
  32. Zigmond AS, Snaith RP. The hospital anxiety and depression scale. Acta Psychiatr Scand 1983; 67: 361–70.[Medline]
  33. Herrmann CH, Buss U, Snaith RP. Psychologisches Screening von Patienten einer kardiologischen Akutklinik mit einer deutschen Fassung der ’84 Hospital Anxiety and Depression (HAD) Scale. Psychother Psychosom Med Psychol 1991; 41: 83–92.[Medline]
  34. Boucsein W. Electrodermal activity. New York: Plenum Press; 1992.
  35. Bode F, Wiegand U, Raasch W, Richardt G, Potratz J. Differential effects of defibrillation on systemic and cardiac sympathetic activity. Heart 1998; 79: 560–7.[Abstract/Free Full Text]
  36. Cook EW. Affective individual differences, psychopathology, and startle reflex modification.In: Dawson ME, Schell AM, Boehmelt AH, editors. Startle modification: implications for neuroscience, cognitive science, and clinical science. New York: Cambridge University Press; 1999.p. 187–208.
  37. Ross RJ, Ball WA, Cohen ME, Silver SM, Morrison AR, Dinges DF. Habituation of the startle reflex in posttraumatic stress disorder. J Neuropsychiatry 1989; 1: 305–7.[Abstract/Free Full Text]
  38. Orr SP, Solomon Z, Peri T, Pitman RK, Shalev A. Physiological responses to loud tones in Israeli veterans of the 1973 Yom Kippur War. Biol Psychiatry 1997; 41: 319–26.[CrossRef][Medline]



This article has been cited by other articles:


Home page
 Psychosom. Med.Home page
J. Baumert, C. Schmitt, and K.-H. Ladwig
Psychophysiologic and Affective Parameters Associated With Pain Intensity of Cardiac Cardioverter Defibrillator Shock Discharges
Psychosom Med, July 1, 2006; 68(4): 591 - 597.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ladwig, K.-H.
Right arrow Articles by Schmitt, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ladwig, K.-H.
Right arrow Articles by Schmitt, C.
Related Collections
Right arrow Stress and Coping
Right arrow Other Cardiovascular Medicine

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS